Abstract
Numerous studies have been conducted regarding association between TNF-α and oral cancer risk, but the results remain controversial. The present meta-analysis is performed to acquire a more precise estimation of relationships. Databases of Pubmed, the Cochrane library and the China National Knowledge Internet (CNKI) were retrieved until August 10, 2013. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated with fixed- or random-effect models. The heterogeneity assumption was assessed by I-squared test. Among the eight included case-control studies, all were focused on TNF-α-308G>A and four also concerned the TNF-α-238G>A polymorphism. It was found that oral cancer risk were significant decreased with the TNF-α-308G>A polymorphism in the additive genetic model (GG vs. AA, OR=0.19, 95% CI: [0.04, 1.00], P=0.05, I2=68.9%) and the dominant genetic model (GG+GA vs. AA, OR=0.22, 95% CI: [0.06, 0.82], P=0.03, I2=52.4%); however, no significant association was observed in allele contrast (G vs. A, OR=0.70, 95% CI: [0.23, 2.16], P=0.54, I2=95.9%) and recessive genetic models (GG vs. GA+AA, OR=0.72, 95% CI: [0.33, 1.57], P=0.41, I2=93.1%). For the TNF-α-238G>A polymorphism, significant associations with oral cancer risk were found in the allele contrast (G vs. A, OR=2.75, 95% CI: [1.25, 6.04], P=0.01, I2=0.0%) and recessive genetic models (GG vs. GA+AA, OR=2.23, 95%CI: [1.18, 4.23], P=0.01, I2=0.0%). Conclusively, this meta-analysis indicates that TNF-α polymorphisms may contribute to the risk of oral cancer. Allele G and the GG+GA genotype of TNF-α- 308G>A may decrease the risk of oral cancer, while allele G and the GG genotype of TNF-α-238G>A may cause an increase.
Highlights
Oral cancer is one of the ten most common cancers in the world and occurs more often to males in developing countries than developed countries (Petersen, 2005; Petersen, 2009; Jemal et al, 2010; Jemal et al, 2011)
Many individuals are exposed to these risk factors, oral cancer develops only in a small group of exposed people, implying that genetic factors may contribute to the carcinogenic mechanisms, and complex interactions between many genetic and environmental factors may be the major cause of oral cancer (Tsigris et al, 2007; Zhuo et al, 2009; Liu et al, 2012a; Miriam et al, 2012)
Inclusion criteria were: (1) case-control studies concerning the association of TNF-α polymorphism with oral carcinoma; (2) studies offering the size of the samples, source of cases and controls, distribution of alleles, genotypes, or other information that could help us infer the results; (3) genetic distribution of the pooled control group was consistent with Hardy-Weinberg equilibrium (HWE)
Summary
Oral cancer is one of the ten most common cancers in the world and occurs more often to males in developing countries than developed countries (Petersen, 2005; Petersen, 2009; Jemal et al, 2010; Jemal et al, 2011). According to the GLOBOCAN 2008 estimates, the incidence of oral cancer for males was listed at ninth worldwide. An estimated 263,900 new cases and 128,000 deaths from oral cavity cancer (including lip cancer) occurred in 2008 worldwide (Jemal et al, 2010). Genetic association studies have estimated the risk of developing a certain malignancy by comparing the frequency of polymorphic genotypes and allele frequencies in cancer patients and health controls. An allele or a genotype is associated with increased risk for neoplasia when its detected frequency is significantly higher in cases than controls (Tsigris et al, 2007; Serefoglou et al, 2008). Several meta-analyses have demonstrated that the Arg194Trp polymorphism in x-ray repair cross-complementing group 1 (XRCC1) gene (Zhou et al, 2009), CYP2E1 RsaI/PstI gene polymorphism (Lu et al, 2011), GSTM1 gene polymorphism (Shukla et al, 2012), and TP53 codon 72 polymorphisms (Zhuo et al, 2009) are related to the susceptibility of oral cancer
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